Enterohemorrhagic Escherichia coli(EHEC) is increasingly recognized as a common cause of both epidemic and sporadic disease, notably bloody diarrhea and hemolytic-uremic syndrome. Common sources of outbreaks have been traced to the consumption of contaminated hamburger, other foods, and drinking water. It was not easy to recover the pathogen from the samples. However, this failure to recover the pathogen may result not because of the absence of the organism, but because the cells entered into what has been termed the viable-but-nonculturable(VBNC) state.Escherichia coli O157 became nonculturable in sterilized distilled water microcosms at low temperature. We could resuscitate the nonculturable cells to inoculate them onto an agar medium amended with catalase or nonenzyme peroxide-degrading compounds such as sodium pyruvate. The proposed mode of action of the catalase or pyruvate is via the degradation of the metabolic by-product H2O2, rather than through supplementation of a required nutrient in the recovery of nonculturable cells. Our studies were based on the assumption that E.coli O157 responds to starvation and a low temperature by entering a nonculturable state and that the correction of oxidative stress during inoculation of bacteria on agar plates, promotes recovery of nonculturable cells. We have also demonstrated that the sigma factor especially sigma 38 of E.coli plays an important role in entering into VBNC state.